From Wikipedia, the free encyclopedia
Chemical compound
Cinaciguat
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Routes of administration |
intravenous (?) |
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ATC code | |
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4-({(4-carboxybutyl)[2-(2-{[4-(2-phenylethyl) phenyl]methoxy}phenyl)ethyl]amino}methyl) benzoic acid
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CAS Number | |
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PubChem
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ChemSpider | |
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ChEBI | |
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CompTox Dashboard (
EPA) | |
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Formula | C36H39NO5 |
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Molar mass | 565.710 g·mol−1 |
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3D model (
JSmol) | |
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c4ccccc4CCc3ccc(cc3)COc1ccccc1CCN(CCCCC(O)=O)Cc2ccc(C(=O)O)cc2
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InChI=1S/C36H39NO5/c38-35(39)12-6-7-24-37(26-30-19-21-33(22-20-30)36(40)41)25-23-32-10-4-5-11-34(32)42-27-31-17-15-29(16-18-31)14-13-28-8-2-1-3-9-28/h1-5,8-11,15-22H,6-7,12-14,23-27H2,(H,38,39)(H,40,41) NKey:WPYWMXNXEZFMAK-UHFFFAOYSA-N N
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NY
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Cinaciguat (BAY 58-2667) is an experimental drug for the treatment of
acute decompensated heart failure.
Mechanism of action
Cinaciguat activates the
soluble guanylate cyclase (sGC) which is a receptor for
nitric oxide. This increases biosynthesis of
cyclic GMP, resulting in
vasodilation.
[1]
See also
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Riociguat, another drug stimulating sGC, but with a different mechanism
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PDE5 inhibitors act further downstream in the nitric oxide signalling pathway, reducing cyclic GMP degradation.
References
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^ Schubert-Zsilavecz, M, Wurglics, M, Neue Arzneimittel 2009
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Forms | |
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Targets | |
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NO donors (
prodrugs) | |
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Enzyme (
inhibitors) | |
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Others |
- Indirect/downstream NO modulators:
ACE inhibitors/
AT-II receptor antagonists (e.g.,
captopril,
losartan)
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ETB receptor antagonists (e.g.,
bosentan)
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L-Type calcium channel
blockers (e.g.,
dihydropyridines:
nifedipine)
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Nebivolol (
beta blocker)
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PDE5 inhibitors (e.g.,
sildenafil)
- non-selective PDE inhibitors (e.g.,
caffeine)
- PDE9 inhibitors (e.g.,
paraxanthine)
- cGMP preferring PDE inhibitors (e.g., sildenafil, paraxanthine, tadalafil)
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Statins (e.g.,
simvastatin)
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